ArticleLife science alliance2025
Efficacy of Nrf2 activation in a proteinuric Alport syndrome mouse model.
Article in Life science alliance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Albumin as a dynamic extracellular redox regulator: from Cys34 oxidation biomarkers to polysulfide-mediated homeostatic mechanisms and clinical applications.Redox report : communications in free radical research · 2026Review
- Accelerated basement membrane remodeling and serum matrix fragments as biomarkers of fibrosis in Alport syndrome.Cell reports · 2026Article
- The AMPK/NRF2/FOXO Axis in CKD-Molecular and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Chronic hyperglycemia and cardiovascular dysfunction: an in-depth exploration of metabolic and cellular pathways in type 2 diabetes mellitus.Cardiovascular diabetology. Endocrinology reports · 2025Review
- Effects of Echinacea Purpurea Polysaccharides on Growth Performance, Serum Biochemistry, and Intestinal Health of Immunosuppressed Broilers.Animals : an open access journal from MDPI · 2025Article
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) has shown protective effects in experimental models of acute kidney injury and nonproteinuric chronic kidney disease. However, the efficacy of Nrf2 activation for proteinuric chronic kidney disease with glomerular injury is controversial, as a transient increase in proteinuria is observed. Here, we identified a potent Nrf2 activator UD-051, which inhibits the interaction between Kelch-like ECH-associated protein 1 (Keap1) and Nrf2. UD-051 significantly ameliorated the progressive phenotype of Alport syndrome mouse model in an Nrf2-dependent manner, accompanied by increased proteinuria. Mild Nrf2 activation by genetic
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